An Economic Approach to the Regulation of Direct Marketing

The growing ubiquity of electronic media and the almost total absence of cost in mass distributions of direct marketing have exacerbated the problem of the increasing intrusion of direct marketing into the privacy of citizens. The Author proposes utilization of a microeconomic social welfare analysis to guide policymakers in determining what forms of direct media should be regulated and what the most effective forms of regulation are likely to be. Sending and receiving costs provide the key factors in determining the extent of the welfare-reducing marketing and marketing aversions, but the Author points to a number of other factors as well, including impact on third parties, impact of economic and technological factors, and changes in volume and targeting in traditional channels. The Author\u27s analysis suggests that increasing the receiver\u27s ability to process information by imposing labeling requirements on distributors could increase welfare without having to resort to the more sweeping and inefficient opt-in or opt-out programs. Many of these solutions can be effectuated by industry and, thus, do not necessarily require government intervention. In the absence of effective industry-based solutions, the Author contends that a complete ban on direct marketing may be required in the electronic media in particular

An Economic Approach to the Regulation of Direct Marketing

The growing ubiquity of electronic media and the almost total absence of cost in mass distributions of direct marketing have exacerbated the problem of the increasing intrusion of direct marketing into the privacy of citizens. The Author proposes utilization of a microeconomic social welfare analysis to guide policymakers in determining what forms of direct media should be regulated and what the most effective forms of regulation are likely to be. Sending and receiving costs provide the key factors in determining the extent of the welfare-reducing marketing and marketing aversions, but the Author points to a number of other factors as well, including impact on third parties, impact of economic and technological factors, and changes in volume and targeting in traditional channels. The Author\u27s analysis suggests that increasing the receiver\u27s ability to process information by imposing labeling requirements on distributors could increase welfare without having to resort to the more sweeping and inefficient opt-in or opt-out programs. Many of these solutions can be effectuated by industry and, thus, do not necessarily require government intervention. In the absence of effective industry-based solutions, the Author contends that a complete ban on direct marketing may be required in the electronic media in particular

Association of Vitamin E Intake at Early Childhood with Alanine Aminotransferase Levels at Mid-Childhood

The extent to which vitamin E (alpha-tocopherol) intake early in childhood is associated with alanine aminotransferase (ALT) level later in childhood is unknown. The objective of this research is to test the hypothesis that higher alpha-tocopherol intake during early childhood is associated with lower odds of elevated ALT levels during mid-childhood, and to examine how body mass index (BMI) influences these relationships. We studied 528 children in Project Viva. Mothers reported child dietary intake at early childhood visits (median 3.1 years) using a validated food frequency questionnaire. At mid-childhood (median 7.6 years), we collected child blood and anthropometric data. The main outcome was elevated sex-specific mid-childhood ALT level (≥ 22.1 units/liter for females and ≥ 25.8 units/liter for males). In multivariable logistic regression models, we assessed the association of energy-adjusted alpha-tocopherol intake with ALT levels, adjusting for child age, sex, race/ethnicity, diet, and age-adjusted, sex-specific BMIz at mid-childhood. Among children in this study, 48% were female, 63% were non-Hispanic white, 19% were non-Hispanic black, and 4% Hispanic/Latino. Mean alpha-tocopherol intake was 3.7±1.0 mg/day (range 1.4-9.2) at early childhood. At mid-childhood, mean BMIz was 0.41±1.0 units and 22% had an elevated ALT level. In multivariable-adjusted logistic regression models, children with higher early childhood vitamin E intake had lower odds of elevated mid-childhood ALT [adjusted odds ratio (AOR) 0.62 (95% CI: 0.39-0.99)] for quartiles 2-4 compared with the lowest quartile of intake. Findings persisted after accounting for early childhood diet [0.62 (0.36, 1.08)] and were strengthened after additionally accounting for mid-childhood BMIz [0.56 (0.32, 0.99)]. Conclusion: In this cohort, higher early childhood intake of alpha-tocopherol was associated with lower odds of elevated mid-childhood ALT level

The Influence of Antenatal Partner Support on Pregnancy Outcomes

BACKGROUND: While there has been considerable attention given to the multitude of maternal factors that contribute to perinatal conditions and poor birth outcomes, few studies have aimed to understand the impact of fathers or partners. We examined associations of antenatal partner support with psychological variables, smoking behavior, and pregnancy outcomes in two socioeconomically distinct prebirth cohorts. MATERIALS AND METHODS: Data were from 1764 women recruited from an urban-suburban group practice (Project Viva) and 877 women from urban community health centers (Project ACCESS), both in the Boston area. Antenatal partner support was assessed by the Turner Support Scale. Multivariable linear and logistic regression analyses determined the impact of low antenatal partner support on the outcomes of interest. RESULTS: In early pregnancy, 6.4% of Viva and 23.0% of ACCESS participants reported low partner support. After adjustment, low partner support was cross-sectionally associated with high pregnancy-related anxiety in both cohorts (Viva AOR 1.8; 95% CI: 1.0-3.4 and ACCESS AOR 1.9; 95% CI: 1.1-3.3) and with depression in ACCESS (AOR 1.9; 95% CI: 1.1-3.3). In Viva, low partner support was also related to depression mid-pregnancy (AOR 3.1; 95% CI: 1.7-5.7) and to smoking (AOR 2.2; 95% CI: 1.3-3.8). Birth weight, gestational age, and fetal growth were not associated with partner support. CONCLUSIONS: This study of two economically and ethnically distinct cohorts in the Boston area highlights higher levels of antenatal anxiety, depression, and smoking among pregnant women who report low partner support. Partner support may be an important and potentially modifiable target for interventions to improve pregnancy outcomes

Residential Proximity to Major Roadways at Birth, DNA Methylation at Birth and Midchildhood, and Childhood Cognitive Test Scores: Project Viva(Massachusetts, USA).

BackgroundEpigenetic variability is hypothesized as a regulatory pathway through which prenatal exposures may influence child development and health.ObjectiveWe sought to examine the associations of residential proximity to roadways at birth and epigenome-wide DNA methylation. We also assessed associations of differential methylation with child cognitive outcomes.MethodsWe estimated residential proximity to roadways at birth using a geographic information system (GIS) and cord blood methylation using Illumina's HumanMethylation450-array in 482 mother-child pairs in Project Viva. We identified individual CpGs associated with residential-proximity-to-roadways at birth using robust linear regression [[Formula: see text]]. We also estimated association between proximity-to-roadways at birth and methylation of the same sites in blood samples collected at age 7-11 y ([Formula: see text]). We ran the same analyses in the Generation R Study for replication ([Formula: see text]). In Project Viva, we investigated associations of differential methylation at birth with midchildhood cognition using linear regression.ResultsLiving closer to major roadways at birth was associated with higher cord blood (and-more weakly-midchildhood blood) methylation of four sites in LAMB2. For each halving of residential-proximity-to-major-roadways, we observed a 0.82% increase in DNA methylation at cg05654765 [95% confidence interval (CI): (0.54%, 1.10%)], 0.88% at cg14099457 [95% CI: (0.56%, 1.19%)], 0.19% at cg03732535 [95% CI: (0.11%, 0.28)], and 1.08% at cg02954987 [95% CI: (0.65%, 1.51%)]. Higher cord blood methylation of these sites was associated with lower midchildhood nonverbal cognitive scores. Our results did not replicate in the Generation R Study.ConclusionsOur discovery results must be interpreted with caution, given that they were not replicated in a separate cohort. However, living close to major roadways at birth was associated with cord blood methylation of sites in LAMB2-a gene known to be linked to axonal development-in our U.S. cohort. Higher methylation of these sites associated with lower nonverbal cognitive scores at age 7-11 y in the same children. https://doi.org/10.1289/EHP2034

Plasma metabolite profiles in children with current asthma

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146270/1/cea13183.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146270/2/cea13183_am.pd

Air Pollution Exposure and Abnormal Glucose Tolerance during Pregnancy: The Project Viva Cohort

Background: Exposure to fine particulate matter (PM with diameter ≤ 2.5 μm; PM2.5) has been linked to type 2 diabetes mellitus, but associations with hyperglycemia in pregnancy have not been well studied. Methods: We studied Boston, Massachusetts–area pregnant women without known diabetes. We identified impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM) during pregnancy from clinical glucose tolerance tests at median 28.1 weeks gestation. We used residential addresses to estimate second-trimester PM2.5 and black carbon exposure via a central monitoring site and spatiotemporal models. We estimated residential traffic density and roadway proximity as surrogates for exposure to traffic-related air pollution. We performed multinomial logistic regression analyses adjusted for sociodemographic covariates, and used multiple imputation to account for missing data. Results: Of 2,093 women, 65 (3%) had IGT and 118 (6%) had GDM. Second-trimester spatiotemporal exposures ranged from 8.5 to 15.9 μg/m3 for PM2.5 and from 0.1 to 1.7 μg/m3 for black carbon. Traffic density was 0–30,860 vehicles/day × length of road (kilometers) within 100 m; 281 (13%) women lived ≤ 200 m from a major road. The prevalence of IGT was elevated in the highest (vs. lowest) quartile of exposure to spatiotemporal PM2.5 [odds ratio (OR) = 2.63; 95% CI: 1.15, 6.01] and traffic density (OR = 2.66; 95% CI: 1.24, 5.71). IGT also was positively associated with other exposure measures, although associations were not statistically significant. No pollutant exposures were positively associated with GDM. Conclusions: Greater exposure to PM2.5 and other traffic-related pollutants during pregnancy was associated with IGT but not GDM. Air pollution may contribute to abnormal glycemia in pregnancy. Citation: Fleisch AF, Gold DR, Rifas-Shiman SL, Koutrakis P, Schwartz JD, Kloog I, Melly S, Coull BA, Zanobetti A, Gillman MW, Oken E. 2014. Air pollution exposure and abnormal glucose tolerance during pregnancy: the Project Viva Cohort. Environ Health Perspect 122:378–383; http://dx.doi.org/10.1289/ehp.130706

Per- and Polyfluoroalkyl Substances and Bone Mineral Density in Mid-childhood

Background: • Identifying factors that impair bone accrual during childhood is a critical step toward osteoporosis prevention. • One potential risk factor not well characterized in childhood is the role of chemicals in the environment. • Perfluoroalkyl substances (PFASs) are synthetic additives used to make clothing, furniture, and cookware stain repellant and are detectable in almost all US adults. • PFASs act as PPAR-γ agonists,2 androgen receptor antagonists, and directly intercalate into bone, raising the possibility that they may lead to low bone accrual. • While two population-based studies in adults have shown associations between PFASs and low areal bone mineral density (aBMD),5,6 the extent to which PFASs may affect aBMD in children is unknown

Maternal corticotropin-releasing hormone is associated with LEP DNA methylation at birth and in childhood: an epigenome-wide study in Project Viva

BackgroundCorticotropin-releasing hormone (CRH) plays a central role in regulating the secretion of cortisol which controls a wide range of biological processes. Fetuses overexposed to cortisol have increased risks of disease in later life. DNA methylation may be the underlying association between prenatal cortisol exposure and health effects. We investigated associations between maternal CRH levels and epigenome-wide DNA methylation of cord blood in offsprings and evaluated whether these associations persisted into mid-childhood.MethodsWe investigated mother-child pairs enrolled in the prospective Project Viva pre-birth cohort. We measured DNA methylation in 257 umbilical cord blood samples using the HumanMethylation450 Bead Chip. We tested associations of maternal CRH concentration with cord blood cells DNA methylation, adjusting the model for maternal age at enrollment, education, maternal race/ethnicity, maternal smoking status, pre-pregnancy body mass index, parity, gestational age at delivery, child sex, and cell-type composition in cord blood. We further examined the persistence of associations between maternal CRH levels and DNA methylation in children's blood cells collected at mid-childhood (n = 239, age: 6.7-10.3 years) additionally adjusting for the children's age at blood drawn.ResultsMaternal CRH levels are associated with DNA methylation variability in cord blood cells at 96 individual CpG sites (False Discovery Rate <0.05). Among the 96 CpG sites, we identified 3 CpGs located near the LEP gene. Regional analyses confirmed the association between maternal CRH and DNA methylation near LEP. Moreover, higher maternal CRH levels were associated with higher blood-cell DNA methylation of the promoter region of LEP in mid-childhood (P < 0.05, β = 0.64, SE = 0.30).ConclusionIn our cohort, maternal CRH was associated with DNA methylation levels in newborns at multiple loci, notably in the LEP gene promoter. The association between maternal CRH and LEP DNA methylation levels persisted into mid-childhood